饮食中的苦生衍生的泽伦可以通过抑制PERK/CHOP依赖的内分泌网膜应激通路在衰老过程中改善记忆性能
Chuan Yang1,2,3, Meihuan Zhao1,2,3, Yuanyuan Chen1,2,3
1State Key Laboratory of Southwestern Chinese Medicine Resources, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China. wen_cdu@163.com.
Food & function
|July 30, 2024
概括
泽伦 (ZB) 通过抑制PERK/CHOP内质网膜应激通路和神经元亡来缓解与衰老相关的认知障碍. 这种天然化合物具有治疗与衰老相关的认知衰退的潜力.
科学领域:
- 神经科学是一个神经科学.
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 与衰老相关的认知衰退 (ARCD) 通过PERK/CHOP通路与内质网膜 (ER) 压力有关.
- 泽伦 (ZB) 是苦中的一种基,具有多种生物活性.
- 通过PERK/CHOP通路对ARCD产生ZB的影响尚不清楚.
研究的目的:
- 为了研究Zerumbone (ZB) 减轻与衰老相关的认知障碍 (ARCD) 的作用和机制.
- 评估ZB抑制PERK/CHOP内质网膜 (ER) 应激通路和神经元亡的能力.
- 评估ZB在D-银糖 (D-gal) 诱导的老化小鼠模型和SH-SY5Y细胞中的疗效.
主要方法:
- 利用D-银糖 (D-gal) 诱导的老化小鼠和SH-SY5Y神经母细胞细胞来模型ARCD和ER压力.
- 管理Zerumbone (ZB) 并评估认知功能,神经元损伤,细胞亡和氧化应激标志物 (MDA,SOD).
- 通过检查GRP78,p-PERK/PERK和CHOP表达来研究PERK/CHOP通路,并使用ER应力调节器 (4-PBA,CCT020312,GSK2606414).
主要成果:
- 泽伦 (ZB) 在体内和体外显著降低了神经元损伤和学习/记忆缺陷.
- ZB抑制了PERK/CHOP通路的激活,降低了GRP78,p-PERK/PERK和CHOP水平,同时减少了氧化损伤.
- ER压力抑制剂 (4-PBA) 逆转了ZB的影响,而PERK激活剂 (CCT020312) 覆盖了它们,PERK抑制剂 (GSK2606414) 增强了它们.
结论:
- 泽伦 (ZB) 通过抑制PERK/CHOP依赖的内分泌网膜应激通路和亡,有效地预防D-银糖诱导的认知缺陷.
- ZB证明了作为治疗老化相关认知障碍 (ARCD) 的治疗剂的潜力.
- 这些发现突出了ZB通过ER应激调制介导的神经保护性质.
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